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LncRNA GACAT1 Promotes Gastric Cancer Cell Growth, Invasion And Migration By Regulating MiR-149-mediated Of ZBTB2 And SP1

Long non-coding RNAs (lncRNAs) were involved in the progression of gastric cancer (GC). In our study, we have determined that GACAT1 expression was upregulated in GC. Overexpression of GACAT1 promoted GC cell proliferation, invasion and migration. We also determined that miR-149 directly interacts w...

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Detalles Bibliográficos
Autores principales: Shi, Xiaoqing, Wang, Xiaoqin, Hua, Yimin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6216017/
https://www.ncbi.nlm.nih.gov/pubmed/30405842
http://dx.doi.org/10.7150/jca.27546
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author Shi, Xiaoqing
Wang, Xiaoqin
Hua, Yimin
author_facet Shi, Xiaoqing
Wang, Xiaoqin
Hua, Yimin
author_sort Shi, Xiaoqing
collection PubMed
description Long non-coding RNAs (lncRNAs) were involved in the progression of gastric cancer (GC). In our study, we have determined that GACAT1 expression was upregulated in GC. Overexpression of GACAT1 promoted GC cell proliferation, invasion and migration. We also determined that miR-149 directly interacts with the target site on GACAT1. Furthermore, we investigated that miR-149 downregulated ZBTB2 and SP1 expressions which were induced by GACAT1, miR-149 inhibited GC cell growth and invasion mediated by GACAT1. In conclusion, we found that miR-149 downregulated ZBTB2 and SP1 expressions, and inhibited GC cell progression mediated by GACAT1. Therefore, we indicated that GACAT1 and miR-149 may be potential therapeutic targets for GC.
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spelling pubmed-62160172018-11-07 LncRNA GACAT1 Promotes Gastric Cancer Cell Growth, Invasion And Migration By Regulating MiR-149-mediated Of ZBTB2 And SP1 Shi, Xiaoqing Wang, Xiaoqin Hua, Yimin J Cancer Research Paper Long non-coding RNAs (lncRNAs) were involved in the progression of gastric cancer (GC). In our study, we have determined that GACAT1 expression was upregulated in GC. Overexpression of GACAT1 promoted GC cell proliferation, invasion and migration. We also determined that miR-149 directly interacts with the target site on GACAT1. Furthermore, we investigated that miR-149 downregulated ZBTB2 and SP1 expressions which were induced by GACAT1, miR-149 inhibited GC cell growth and invasion mediated by GACAT1. In conclusion, we found that miR-149 downregulated ZBTB2 and SP1 expressions, and inhibited GC cell progression mediated by GACAT1. Therefore, we indicated that GACAT1 and miR-149 may be potential therapeutic targets for GC. Ivyspring International Publisher 2018-09-08 /pmc/articles/PMC6216017/ /pubmed/30405842 http://dx.doi.org/10.7150/jca.27546 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Shi, Xiaoqing
Wang, Xiaoqin
Hua, Yimin
LncRNA GACAT1 Promotes Gastric Cancer Cell Growth, Invasion And Migration By Regulating MiR-149-mediated Of ZBTB2 And SP1
title LncRNA GACAT1 Promotes Gastric Cancer Cell Growth, Invasion And Migration By Regulating MiR-149-mediated Of ZBTB2 And SP1
title_full LncRNA GACAT1 Promotes Gastric Cancer Cell Growth, Invasion And Migration By Regulating MiR-149-mediated Of ZBTB2 And SP1
title_fullStr LncRNA GACAT1 Promotes Gastric Cancer Cell Growth, Invasion And Migration By Regulating MiR-149-mediated Of ZBTB2 And SP1
title_full_unstemmed LncRNA GACAT1 Promotes Gastric Cancer Cell Growth, Invasion And Migration By Regulating MiR-149-mediated Of ZBTB2 And SP1
title_short LncRNA GACAT1 Promotes Gastric Cancer Cell Growth, Invasion And Migration By Regulating MiR-149-mediated Of ZBTB2 And SP1
title_sort lncrna gacat1 promotes gastric cancer cell growth, invasion and migration by regulating mir-149-mediated of zbtb2 and sp1
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6216017/
https://www.ncbi.nlm.nih.gov/pubmed/30405842
http://dx.doi.org/10.7150/jca.27546
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